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Wolverhampton Intellectual Repository and E-Theses > Research Institutes > Research Institute in Healthcare Science > Cancer Research Group > Spectrum of copy number changes in low grade paediatric brain tumours detected by comparative genomic hybdidisation

Please use this identifier to cite or link to this item: http://hdl.handle.net/2436/30199
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Title: Spectrum of copy number changes in low grade paediatric brain tumours detected by comparative genomic hybdidisation
Other Titles: In: Abstracts from the 14th International Conference on Brain Tumor Research and Therapy. Asheville, North Carolina, USA. May 27-30, 2001. No.180
Authors: Warr, Tracy
Ward, Samantha
Idowu, Michael O.
Gregory, S.
Darling, John L.
Thomas, David G.
Citation: Neuro-oncology, 3(Suppl 1): 310
Publisher: Society for Neuro-Oncology and Duke University Press
Journal: Neuro-oncology
Issue Date: 2001
URI: http://hdl.handle.net/2436/30199
Additional Links: http://neuro-oncology.dukejournals.org/
http://www.pubmedcentral.nih.gov/tocrender.fcgi?iid=145976
Abstract: Several different types of low-grade brain tumours arise predominantly in the paediatric population, including astrocytoma, craniopharygioma and choroid plexus papilloma (CPP). As yet, the genetic events that contribute to their development have not been well defined. We have used comparative genomic hybridisation (CGH) to identify regions of genetic loss and gain in a series of 30 low grade tumours comprising 7 pilocytic astrocytoma (WHO grade I), 12 grade II astrocytoma, 5 craniopharyngioma (WHO grade I) and 6 CPP (WHO grade I). In the group of astrocytoma, there were no detectable regions of genomic imbalance in all 7 grade I tumours and in 9 of 12 grade II tumours. The copy number changes in the remaining 3 cases of grade II astrocytoma were gain of 7p and 12p; loss of 1p, 12q and 22; gain of 2q, 3, 8q and 18q, respectively. Similarly, 4 of 5 craniopharyngioma appeared to have normal CGH profiles, although multiple changes including gain of 4, 6q, 8q and 18q and loss of 17, 20q and 22 were observed in the sixth case. In contrast, copy number aberrations were detected in 3 of 6 CPP. In one tumour, gain of 7 was the sole change, whereas gain of 3q and 6q and loss of 9q and 21 were detected in a second case. However, in the remaining CPP all chromosomes except X and Y were involved in copy number changes with gain of 1, 7, 9, 12, 15, 16, 18, 20 and 22 and loss of the remaining autosomes. Overall, genomic imbalance was detected in only 7 of these low grade tumours and it was not possible to identify consistent regions of loss and gain. Considerably larger numbers of each tumour type need to be analysed in order to elucidate the genetic pathways involved in tumourigenesis.
Type: Meetings & Proceedings
Language: en
Description: Abstracts from Neuro-Oncology are provided here courtesy of Society for Neuro-Oncology and Duke University Press.
Keywords: Oncology
Paediatric tumours
Brain Tumours
Genomics
CGH
Comparative Genomic Hybridisation
Astrocytoma
Craniopharyngioma
Chromosomal Aberrations
Choroid plexus
ISSN: 1522-8517
Appears in Collections: Cancer Research Group

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